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This Committee Report provides methodological, interpretive, and reporting guidance for researchers who use measures of heart rate (HR) and heart rate variability (HRV) in psychophysiological research. We provide brief summaries of best practices in measuring HR and HRV via electrocardiographic and photoplethysmographic signals in laboratory, field (ambulatory), and brain‐imaging contexts to address research questions incorporating measures of HR and HRV. The Report emphasizes evidence for the strengths and weaknesses of different recording and derivation methods for measures of HR and HRV. Along with this guidance, the Report reviews what is known about the origin of the heartbeat and its neural control, including factors that produce and influence HRV metrics. The Report concludes with checklists to guide authors in study design and analysis considerations, as well as guidance on the reporting of key methodological details and characteristics of the samples under study. It is expected that rigorous and transparent recording and reporting of HR and HRV measures will strengthen inferences across the many applications of these metrics in psychophysiology. The prior Committee Reports on HR and HRV are several decades old. Since their appearance, technologies for human cardiac and vascular monitoring in laboratory and daily life (i.e., ambulatory) contexts have greatly expanded. This Committee Report was prepared for the Society for Psychophysiological Research to provide updated methodological and interpretive guidance, as well as to summarize best practices for reporting HR and HRV studies in humans. [ABSTRACT FROM AUTHOR]

Resting heart rate may confer risk for cardiovascular disease (CVD) and other adverse cardiovascular events. While the brainstem's autonomic control over heart rate is well established, less is known about the regulatory role of higher level cortical and subcortical brain regions, especially in humans. This study sought to characterize the brain networks that predict variation in prevailing heart rate in otherwise healthy adults. We used machine learning approaches designed for complex, high‐dimensional data sets, to predict variation in instantaneous heart period (the inter‐heartbeat‐interval) from whole‐brain hemodynamic signals measured by fMRI. Task‐based and resting‐state fMRI, as well as peripheral physiological recordings, were taken from two data sets that included extensive repeated measurements within individuals. Our models reliably predicted instantaneous heart period from whole‐brain fMRI data both within and across individuals, with prediction accuracies being highest when measured within‐participants. We found that a network of cortical and subcortical brain regions, many linked to visceral motor and visceral sensory processes, were reliable predictors of variation in heart period. This adds to evidence on brain–heart interactions and constitutes an incremental step toward developing clinically applicable biomarkers of brain contributions to CVD risk. Using whole‐brain fMRI data, we reliably predicted instantaneous heart period within and across individuals from the activity of a network of cortical and subcortical brain regions, many linked to visceral motor and visceral sensory processes. This adds to existing evidence on brain–heart interactions and constitutes a step toward developing clinically applicable biomarkers of brain contributions to CVD risk. [ABSTRACT FROM AUTHOR]

Threats to social connectedness in the form of social and societal rejection, and the permanent loss of social bonds, are inevitable and common sources of social pain. However, sensitivity to social pain, also known as algesia, differs across individuals and contexts. Such sensitivity has implications for health, well-being, and the maintenance of social connection over time. What biological factors predict differences in sensitivity to social pain? Based on long-standing translational perspectives and emerging findings, the current review highlights blood pressure as a novel predictor of sensitivity to social pain: Higher resting blood pressure appears to relate to lower sensitivity to social pain. Despite evidence for this association, possible psychobiological bases and moderating influences are not yet established. Moreover, although higher blood pressure may afford tolerance for life's many pains, the health-related implications and trade-offs of such an effect are unknown. [ABSTRACT FROM AUTHOR]

In a midlife sample of adults, the present study tested the extent to which changes in psychological stress relate to the progression of subclinical cardiovascular disease over multiple years and explored the potential moderating role of cardiometabolic risk. Method: Participants were screened to exclude those with clinical cardiovascular, respiratory, metabolic, and other chronic illnesses, as well as those taking psychotropic, cardiovascular, lipid, and glucose control medications. At baseline (N = 331) and then again at follow-up an average of 3 years later (N =260), participants completed the 10-item Perceived Stress Scale, underwent assessments of their cardiometabolic risk, and underwent ultrasonography to measure carotid artery intima-media thickness (IMT), which is a surrogate indicator of subclinical atherosclerosis. Results: Regression models showed that the change in psychological stress from baseline to follow-up was positively associated with the corresponding change in IMT, with covariate control for age at baseline, sex at birth, and variability in length of follow-up across participants. Cardiometabolic risk factors did not statistically moderate this longitudinal association. In exploratory analyses, cardiometabolic risk factors also did not statistically mediate this association. Conclusion: These longitudinal findings suggest that increases in psychological stress in midlife relate to corresponding increases in subclinical atherosclerosis. [ABSTRACT FROM AUTHOR]

Background Subjective social status (SSS) refers to a person's perception of their social rank relative to others and is cross-sectionally linked to systemic inflammation independently of objective socioeconomic status. Purpose We test the extent to which SSS relates to multiyear changes in inflammation, or if associations differ by race or sex. Methods Healthy adults (N = 331; 30–51 years) completed a baseline visit and 278 participants returned for a second visit 2.85 years later. At both visits, participants underwent a fasting blood draw and completed community (SSSC) and US (SSSUS) versions of the MacArthur Scale. Multiple linear regression analyses examined change in interleukin-6 (IL-6) and C-reactive protein (CRP) predicted by each type of SSS, adjusting for time between visits, sex, race, age, body mass index, smoking, baseline inflammation, and objective socioeconomic status. Additional analyses further adjusted for hopelessness and depressive symptoms. Interactions examined moderations by sex and race. Results Lower SSSC was longitudinally associated with greater IL-6 independently of all covariates, including education and income (β = −0.06), hopelessness (β = −0.06), and depressive symptoms (β = −0.06). Lower SSSUS was longitudinally associated with greater IL-6 independently of demographic covariates including education and income (β = −0.06), but was slightly attenuated after adjusting for hopelessness (β = −0.06) and depressive symptoms (β = −0.06). There were no associations for CRP or moderation by race or sex. Conclusions Lower SSS may be associated with greater circulating markers of inflammation over time as suggested by increases in IL-6. [ABSTRACT FROM AUTHOR]

Background: Chronic exposure to air pollution may prime the immune system to be reactive, increasing inflammatory responses to immune stimulation and providing a pathway to increased risk for inflammatory diseases, including asthma and cardiovascular disease. Although long-term exposure to ambient air pollution has been associated with increased circulating markers of inflammation, it is unknown whether it also relates to the magnitude of inflammatory response. Objectives: The aim of this study was to examine associations between chronic ambient pollution exposures and circulating and stimulated levels of inflammatory mediators in a cohort of healthy adults. Methods: Circulating interleukin (IL)-6, C-reactive protein (CRP) (n = 392), and lipopolysaccharide stimulated production of IL-1[beta], IL-6, and tumor necrosis factor (TNF)-[alpha] (n = 379) were measured in the Adult Health and Behavior II cohort. Fine particulate matter [particulate matter with aerodynamic diameter less than or equal to 2.5 [micro]m ([PM.sub.2.5])] and constituents [black carbon (BC), and lead (Pb), manganese (Mn), zinc (Zn), and iron (Fe)] were estimated for each residential address using hybrid dispersion land use regression models. Associations between pollutant exposures and inflammatory measures were examined using linear regression; models were adjusted for age, sex, race, education, smoking, body mass index, and month of blood draw. Results: There were no significant correlations between circulating and stimulated measures of inflammation. Significant positive associations were found between exposure to [PM.sub.2.5] and BC with stimulated production of IL-6, IL-1[beta], and TNF-[alpha]. Pb, Mn, Fe, and Zn exposures were positively associated with stimulated production of IL-1[beta] and TNF-[alpha]. No pollutants were associated with circulating IL-6 or CRP levels. Discussion: Exposure to [PM.sub.2.5], BC, Pb, Mn, Fe, and Zn was associated with increased production of inflammatory mediators by stimulated immune cells. In contrast, pollutant exposure was not related to circulating markers of inflammation. These results suggest that chronic exposure to some pollutants may prime immune cells to mount larger inflammatory responses, possibly contributing to increased risk for inflammatory disease. https://doi.org/10.1289/EHP7089, Introduction Exposure to airborne fine particulate matter [particulate matter with aerodynamic diameter less than or equal to 2.5 [micro]m ([PM.sub.2.5])] has been associated with increased risk of cardiopulmonary diseases, and [...]

Physical activity (PA) in the form of aerobic exercise (AE) preserves and improves neurocognitive function across the lifespan. However, a mechanistic understanding of the pathways by which aerobic exercise impacts brain health is still lacking, particularly with respect to stress-related pathways. One mechanistic hypothesis is that AE improves neurocognitive health in part by modifying circulating levels of stress-related hormones and signaling factors associated with the hypothalamic-pituitary-adrenal (HPA) axis and autonomic nervous system (ANS), as commonly measured by the biomarkers cortisol (CORT) and salivary α-amylase (sAA). Thus, this hypothesis predicts that changes in stress biomarkers, such as CORT and sAA, are possible explanatory pathways mediating the positive effects of AE on neurocognitive health. In the present review article, we provide a summary of available studies examining the possibility that exerciseinduced changes to stress biomarkers could partly account for exercise-related improvements in neurocognitive health. Our review indicates that despite the intuitive appeal of this hypothesis, there is insufficient evidence available to conclude that chronic and habitual AE affects neurocognitive health by altering stress biomarker pathways. The cross-sectional nature of the majority of reviewed studies highlights the need for well-controlled studies to adequately test this hypothesis. [ABSTRACT FROM AUTHOR]

Childhood trauma may confer risk for poorer adult health through changes in systemic inflammation. Emotion regulation may plausibly moderate associations between childhood trauma and adult psychological well‐being, but it remains unclear whether moderation effects extend to differences in systemic inflammation. To examine whether childhood trauma and emotion regulation separately and interactively predict prospective changes in C‐reactive protein (CRP) and interleukin‐6 (IL‐6) and whether biopsychosocial factors account for observed associations. Healthy midlife adults (N = 331) retrospectively reported on childhood trauma, current trait‐level cognitive reappraisal and expressive suppression, and had their blood drawn. At baseline and then a median of 2.85 years later, 279 of the 331 participants had their blood drawn, body mass index calculated, and reported on health behaviours (smoking, sleep), psychological distress (perceived stress, depressive symptoms), and years of education. Childhood trauma predicted prospective increases in CRP (B = 0.004, p = 0.049), which were partially accounted for by differences in adiposity, psychological distress, and health behaviours. In contrast, cognitive reappraisal predicted prospective decreases in IL‐6 (B = −0.007, p = 0.006), which were independent of biopsychosocial influences. Cognitive reappraisal further moderated the association between childhood trauma and prospective changes in IL‐6 (B = −0.001, p = 0.012) such that childhood trauma predicted greater IL‐6 increases but only among adults lower in cognitive reappraisal (B = 0.006, p = 0.007). There were no main or moderation effects of expressive suppression (ps > 0.05). Cognitive reappraisal may attenuate IL‐6 changes over time and may moderate the prospective association between childhood trauma and systemic inflammation in midlife. [ABSTRACT FROM AUTHOR]

Background: Several personality traits increase the risk for atherosclerotic cardiovascular disease. Because many of these traits are correlated, their associations with disease risk could reflect shared variance, rather than unique contributions of each trait. We examined a higher‐order personality trait of Stability as related to preclinical atherosclerosis and tested whether any such relationship might be explained by correlated variation in cardiometabolic risk factors. Method: Among 798 community volunteers, lower‐order traits of Neuroticism, Agreeableness, and Conscientiousness were modeled as latent variables (from self‐ and informant ratings) and used to estimate the second‐order factor, Stability. Cardiometabolic risk was similarly modeled from indicators of glycemic control, blood pressure, adiposity, and lipids. Carotid artery atherosclerosis was measured as intima‐media thickness (IMT) by duplex ultrasonography. Result: A structural equation model incorporating direct and indirect effects showed lower Stability associated with greater IMT, and this relationship was accounted for by the indirect pathway via cardiometabolic risk. Secondary analyses showed that: (1) Neuroticism, Agreeableness, and Conscientiousness were unrelated to IMT independent of Stability; and (2) Stability predicted variation in IMT when estimated from informant‐, but not self‐rated, traits. Conclusion: Personality traits may associate with atherosclerotic burden through their shared, rather than unique, variance, as reflected in Stability. [ABSTRACT FROM AUTHOR]

In response to the COVID‐19 pandemic, prior studies have modified the Trier Social Stress Test to be conducted remotely. The current study aimed to extend these studies to test whether a remote Trier Social Stress Test (rTSST) can elicit (a) affective, (b) blood pressure, and (c) heart rate responses relative to a control condition and whether these responses were reliable when assessed 1 week later. Participants (N = 99, 19.7 ± 3.5 years, 55% female) were randomized to a control or stress condition. Participants received blood pressure monitors in person. Controls completed easier versions of the tasks with a single, friendly researcher. Stress participants performed more difficult versions of the task in front of two judges who participants believed were rating their performance. Blood pressure and heart rate were measured every 2 min throughout, while affect was assessed at baseline, after the final task, and following recovery. The rTSST was feasible to administer with minimal technical issues reported. Participants reported lower positive affect and higher negative affect during the tasks in the stress condition relative to controls. Similarly, stress participants had higher cardiovascular responses during the tasks relative to controls, except that blood pressure was not elevated during mental arithmetic in stress participants relative to controls. Cardiovascular responses demonstrated good test–retest reliability when assessed 1 week later, especially when computed using area under the curve methods. Overall, a rTSST can be used to elicit affective and cardiovascular reactivity and provides an opportunity to increase the accessibility of research participation among diverse populations. We demonstrate that the Trier Social Stress Test can evoke both affective and cardiovascular (heart rate and blood pressure) responses when delivered online and remotely. This protocol can be administered during the COVID‐19 pandemic and could be used to include underserved and other populations that may have less accessibility to participate in research protocols. [ABSTRACT FROM AUTHOR]

Social pain is a common experience that has potent implications for health. However, individuals differ in their sensitivity to social pain. Recent evidence suggests that sensitivity to social pain varies according to a biological factor that modulates sensitivity to physical pain: resting (tonic) blood pressure. The current studies extended this evidence by testing whether blood pressure relates to sensitivity to imagined (Study 1: N = 762, 51% female adults) and acute (Study 2, preregistered: N = 204, 57% female adults) experiences of social pain and whether associations extend to general emotional responding (Studies 1–3; Study 3: N = 162, 59% female adults). In line with prior evidence, results showed that higher resting blood pressure was associated with lower sensitivity to social pain. Moreover, associations regarding blood pressure and sensitivity to social pain did not appear to be explained by individual differences in general emotional responding. Findings appear to be compatible with the interpretation that social and physical pain share similar cardiovascular correlates and may be modulated by convergent interoceptive pathways. [ABSTRACT FROM AUTHOR]